Understanding circadian clock genes in ageing and cognition

The overall aim of this project is to identify the molecular basis of how circadian rhythms alter with age and ultimately whether a biological mechanism can be identified to prolong healthy circadian rhythms into old age. At the cellular level the generation of self-sustained circadian rhythms is produced via "clock genes" such as Period (Per), Clock (Clk), Cryptochrome (Cry) and Brain muscle ARNT-like1 (Bmal1). A series of Interlocking transcriptional/translational feedback loops involving these genes generate and sustain these rhythms. An association between clock genes and ageing has been suggested by studies in genetically modified mice. We have identified abnormal circadian activity with increasing age in mice. We have also found similar abnormality in circadian rhythms in locomotor activity accompanied by altered expression in brain of circadian genes such as Per and Cry in a transgenic mouse model for Alzheimer's disease. There many questions to be investigated, for example how is clock gene expression altered with age? Are the behavioural patterns associated with reduced clock gene expression ? does age affect the rhythm of other behaviours such as memory ? Reading : Banks et al., 2017 Mammalian genome 27: 332-340. Oyegbami et al, 2017 Current Alzheimer Research 8 : 850-860.